The hepcidin-ferroportin axis controls the iron content of Salmonella-containing vacuoles in macrophages

Daejin Lim, Kwang Soo Kim, Jae-Ho Jeong, Oriana Marques, Hyun-Ju Kim, Miryoung Song, Tae-Hoon Lee, Jae Il Kim, Hueng-Sik Choi, Jung-Joon Min, Dirk Bumann, Martina U. Muckenthaler and Hyon E. Choy ()
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Daejin Lim: Chonnam National University Medical School
Kwang Soo Kim: Chonnam National University Medical School
Jae-Ho Jeong: Chonnam National University Medical School
Oriana Marques: Oncology and Immunology - University of Heidelberg
Hyun-Ju Kim: Chonnam National University Medical School
Miryoung Song: Chonnam National University Medical School
Tae-Hoon Lee: Chonnam National University Graduate School
Jae Il Kim: Gwangju Institute of Science and Technology
Hueng-Sik Choi: Chonnam National University
Jung-Joon Min: Chonnam National University Graduate School
Dirk Bumann: University of Basel
Martina U. Muckenthaler: Oncology and Immunology - University of Heidelberg
Hyon E. Choy: Chonnam National University Medical School

Nature Communications, 2018, vol. 9, issue 1, 1-12

Abstract: Abstract Macrophages release iron into the bloodstream via a membrane-bound iron export protein, ferroportin (FPN). The hepatic iron-regulatory hormone hepcidin controls FPN internalization and degradation in response to bacterial infection. Salmonella typhimurium can invade macrophages and proliferate in the Salmonella-containing vacuole (SCV). Hepcidin is reported to increase the mortality of Salmonella-infected animals by increasing the bacterial load in macrophages. Here we assess the iron levels and find that hepcidin increases iron content in the cytosol but decreases it in the SCV through FPN on the SCV membrane. Loss-of-FPN from the SCV via the action of hepcidin impairs the generation of bactericidal reactive oxygen species (ROS) as the iron content decreases. We conclude that FPN is required to provide sufficient iron to the SCV, where iron serves as a cofactor for the generation of antimicrobial ROS rather than as a nutrient for Salmonella.

Date: 2018
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DOI: 10.1038/s41467-018-04446-8

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